Using a Herpes Medication to Combat HIV Activity

A herpes medication can reduce human immunodeficiency virus (HIV) levels no matter a patient’s herpes status, according to research published in the journal Clinical Infectious Diseases.

Researchers from Case Western Reserve University observed 18 HIV infected herpes patients that were randomly assigned to receive either twice daily valacylovir 500 mg or a placebo for 12 weeks. The researchers aimed to determine whether valacylovir (sold under the name Valtrex) would suppress viral load in this patient population. The patients had CD4 cell counts ≥500 cells/µL and were not taking antiretroviral therapy medication. The first group of patients received 12 weeks of valacyclovir 500 mg given twice daily by mouth, followed by 2 weeks of no treatment, followed by 12 weeks of a placebo. The subjects in the other group received the same treatment, but in reverse order.

The researchers noted that prior research demonstrated that the anti-herpetic drug acyclovir had the ability to suppress herpes and reduce viral load in HIV patients. This was believed to be due to a decrease in overall immune activation, and the researchers wanted to measure this effect using ex vivo tissue samples from herpes infected HIV patients.

The researchers found that after the study period, the plasma of patients treated with valacylovir 500 mg twice daily for 12 weeks had been reduced by an average of 0.37 log₁₀ copies/ mL. When patients took the placebo, their viral loads increased.

“These results demonstrated that the mechanism by which valacyclovir acts against HIV is not only through the presence of herpes,” senior author Benigno Rodriguez, MD, explained in a press release. The participant groups helped demonstrate the specific way that the valacyclovir works to decrease HIV activity levels. Valacyclovir is activated in the virus infected cells, the authors said, and then blocks the ability of the HIV cells to reproduce. This reduces viral load overall.

The research team hopes that in the future, the data from this study can shape new drug development for blocking HIV activity. The authors believe they can use this new information to design agents similar to valacyclovir.

“Our most recent clinical study demonstrates that acyclovir blocks HIV replication directly,” Michael M. Lederman, MD, another senior author, continued in the statement. “The anti-HIV activity of valacyclovir does not depend on blocking the inflammation caused by herpes simplex virus 2. The drug might be an agent that can be used safely in some people with HIV infection who have a form of HIV that is highly resistant to other antiretroviral drugs. Valacyclovir might well augment the cocktail of medications they take for reducing HIV replication. Valacyclovir is a well-tolerated drug, and it doesn't have a lot of side effects.”